Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

Vascular Calcification-New Insights Into Its Mechanism.

Sjogren's syndrome: An update on disease pathogenesis, clinical manifestations and treatment.

An ideal tool for all radiology residents and students, it covers all subspecialty areas and current imaging modalities as utilized in neuroradiology, chest, breast, abdominal, musculoskeletal imaging, ultrasound, pediatric imaging, interventional techniques and nuclear radiology. New and expanded topics in this edition include use of diffustion-weighted MR, new contrast agents, breast MR, and current guidelines for biopsy and intervention. Many new images, expanded content, and full-color throughout make the fourth edition of this classic text a comprehensive review that is ideal as a first reader for beginning residents, a reference during rotations, and a vital resource when preparing for the American Board of Radiology examinations.

Fundamentals of Diagnostic Radiology

https://cyberleninka.org/article/n/675468.pdf

Serum uric acid and acute kidney injury: A mini review

Key Clinical Message
Calcific uremic arteriolopathy or calciphylaxis is a rare and potentially fatal condition, which manifests as skin ischemia and necrosis, usually seen in patients with end-stage renal disease. It is frequently associated with vascular calcification visible on plain radiographs, which can occur in various patterns.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ccr3.1220

Patterns of vascular calcification in patients with end-stage renal disease and calcific uremic arteriolopathy.

Objectives: We investigated the effects of nesiritide (NES) on inflammatory response during cardiac surgery Materials and Methods: Twenty-nine cardiac surgery patients were randomized to an infusion of NES at 001 mcg/kg/min for 48 h versus placebo (Ctrl) A panel of candidate biomarkers and clinical parameters were measured at predetermined time points Results: There were no significant differences between the groups with regard to urine neutrophil gelatinase-associated lipocalin (NES 2303 + 715 ng/mL vs Ctrl 5544 + 2633 ng/mL, P = 0253) and urine interleukin (IL)-18 (NES 299 + 48 pg/mL vs 2545 + 1183 pg/mL, P = 0090), or to the incidence of acute kidney injury (NES 71% vs Ctrl 133%, P = 0374) A concerted biomarker kinetic pattern of time-differentiated peak concentrations was observed IL-10, inflammatory protein (IP)-10, IL-6, IL-10, IP-10, monocyte IP (MIP)-1α, interferon (IFN)-α, IFN-α, IL-1a, IL-3, and IL-7 reached peak concentration at 0 h following the end of cardiopulmonary bypass; tumor necrosis factor (TNF)-α, endothelial growth factor (EGF), granulocyte macrophage-colony-stimulating factor (GM-CSF), IL-12p40, IL-17, MIP-1α, and monocyte chemoattractant protein-1 at 1 h; IL-18, vascular EGF (VEGF), IL-13 and IL-1ra at 2 h, TNF-α, G-CSF, IL-1b, IL-2, IL-4, IL-5, and IL-15 at 4 h; and endothelin (ET)-1 and IL-18 at 6 h At 0 h, the NES group exhibited significant reduction of peak concentrations of IL-6 (P = 0009), IL-10 (P = 0009), IL-1α (P = 0020), IP-10 (P = 0001), and IFN-α (P = 0032) compared to the Ctrl group Significant reduction in peak concentrations of TNF-α (P = 0007) and MIP1-α (P = 0027) at 1 h and ET-1 (P = 0020) at 6 h in the NES group compared to the Ctrl group was noted Conclusion: NES modulated the concerted inflammatory response in cardiac surgery and also attenuated ET-1 response, thus suggesting that previously observed favorable renal effect may be linked to reduced renal vasoconstriction

Nesiritide modulates inflammatory response during cardiac surgery: A pilot study

To the Editor It is well known that successful kidney transplantation is associated with improved quality of life, improved survival and decreased health care cost burden compared to dialysis. Although the overall risk of ESRD is minimal after kidney donation [1], transplant centers across the world vary widely in their acceptance criteria for living kidney donation in the absence of epidemiologic data for the assessment of patient-specific long-term risk in donors. In a recent retrospective analysis involving 133,824 living kidney donors, Massie et al. have found that the 20-year risk of ESRD is significantly high in certain donor groups (up to 8 times) compared to average-risk donors. These groups included males, blacks, those biologically related to their recipients, and obese and older individuals [2]. In addition to utilizing this valuable information, incorporation of a more objective method such as estimation of renal functional reserve (RFR) could serve as an excellent clinical tool for the risk stratification of potential kidney donors. RFR is a well-described but underexplored concept that is defined as the difference between stress glomerular filtration rate (GFR) and baseline GFR. Stress GFR is the supranormal GFR that represents the reserve capacity of the kidney to increase GFR in response to certain physiologic or pathologic stimuli, which can be clinically elicited by administering a protein load [3]. Acute kidney injury (AKI) may damage a variable number of nephrons, and in a person with intact RFR, up to 50% of the nephrons can be damaged while the baseline GFR and serum creatinine remain within the normal range [4]. Such patients may partially or completely lose their RFR depending on the severity of AKI and still be classified as having ‘normal’ renal function, which increases their risk for further kidney injury or ESRD after kidney donation. This is similar to the finding that pregnant women with history of recovered AKI are at increased risk for preeclampsia and adverse fetal outcomes despite normal GFR, which is likely due to their loss of RFR [5]. As such, measuring the RFR prior to kidney donation, particularly in the above-mentioned highrisk groups may help identify individuals with increased risk of developing chronic kidney disease and progression to ESRD. In this context, it is interesting to note that a recent single-center pilot study has shown that the RFR measured preoperatively in living kidney donors was not preserved after transplantation [6]. Future larger studies should focus on exploring this clinical tool further and possibly developing simplified protocols for RFR testing.

Renal functional reserve: time to find a new bottle for the old wine?

Bullous pemphigoid has been linked to allograft rejection, as well as membranous nephropathy in renal transplant recipients. Although there is a possibility of multiple distinct autoimmune processes, immune stimulation induced by allograft rejection or antibasement zone antibody interactions are possible mechanisms for the simultaneous skin and renal involvement.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ccr3.1324

Abhilash Koratala

Papers

Patterns of vascular calcification in patients with end-stage renal disease and calcific uremic arteriolopathy.

Nesiritide modulates inflammatory response during cardiac surgery: A pilot study

Renal functional reserve: time to find a new bottle for the old wine?

The skin-kidney connection: bullous pemphigoid associated with acute allograft rejection and membranous nephropathy.

Point of Care Ultrasonography Enhanced Physical Examination: A Nephrologist's Perspective